1/18
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced |
---|
No study sessions yet.
Lactate threshold
as exercise intensity increases during an incremental exercise test blood levels of lactate rise exponentially
appress at 50-60% VO2 max in untrained individuals
higher work rates in trained individuals 65-80% VO2 max
as acidosis changes
shift in ATP
stimulate glycolytic pathway
AMP stimulates glycolysis
incremental exercise
measure in blood
switch will move LDL in that direction
increase free fatty avid metabolism
protein coupled receptors
OBLA
onset of blood lactate accumulation
Differs from lactate threshold as it is not a blood lactate inflection point but instead the exercise intensity at which a specific blood lactate concentration is reached
lactate threshold vs anaerobic threshold
anaerobic threshold is sudden rise in blood lactate concentration whereas LT is the incremental rise in lactate threshold is a measurable physiological point where lactate production exceeds removal
2 intensities
mitigate or alter start of LT
want to control intensities until this point
within OBLA
anaerobic threshold
CO2 potent vasodilator of coronary and cerebral arteries
CO2 drops and blood flow may begin to drop
delivery is more than flow
flow X O2 []
high intensity exercise training on lactate/H transport capacity
single leg exercise 3x/week for 1st 5 weeks then 5x/week for following 3 weeks
8 weeks of single leg training
resistance standardized based on Newtons
plasma blood lactate increased
increase peak power, mean power, endurance
systems were more efficient at producing lactate
better at using glycolytic system
increase in MCTs [] increase in lactate
results
improved lactate and H transport
MCT and HAD
improved anaerobic and aerobic performance
improved isometric force
no change in bicarbonate
increase carbonic anhydrase
more efficient in moving CO2
practical uses of lactate threshold
anaerobic threshold
classic term used to describe the intensity / work load at which anaerobic metabolism became prevalent
was used synonymous with LT
lactate threshold
point at which blood lactate levels being to rise exponentially during exercise (50-60% VO2 max)
maximal lactate at steady state
maximal lactate achieved at steady state workload
critical power
point at which workload can me maintained at a steady state
metabolic response is different for each individual leading to different genetic expression
exercise at different relative percentage of output
different absolute workloads
differences in substrate utilization
glucose, lipid, lactate, ketone
not a macromolecule
cross-over concept
As intensity increases progressive increase in CHO metabolism and decrease in Lipid metabolism
there is an intensity at which the energy derived from CHO exceeds that of fat
This point is the cross-over point
Recruitment of fast fibres and increasing blood levels of epinephrine causes this shift from fat to carbohydrate
The abundance of glycolytic enzymes in type 2 fibres but few mitochondrial and lipolytic enzymes
Better equipped to metabolize CHO than fats
Increased recruitment results in greater CHO metabolism and less fat metabolism
Epinephrine increases a progressive rise in blood levels of epinephrine
High level of epinephrine increases phosphorylase activity causing an increase in muscle glycogen breakdown
Increased rate of glycolysis and lactate production
Inhibits fat metabolism by reducing availability of fat as a substrate
This makes CHO the primary fuel
longer production increases fatty acid beta oxidization
exercise duration and fuel selection
Prolonged moderate exercise (greater than 30 mins) the R decreases over time
Indicates gradual shift form CHO metabolism toward and increasing reliance on it as substrate
rates of glycogen breakdown for various exercise intensities
Heavier the exercise the faster glycogen is broken down
Initiated by second messengers which activate protein kinase in the muscle cell
Plasma epinephrine
Stimulator of cAMP formation when bound to beta-adrenergic receptors was believed to be primarily responsible for glycogenolysis
exercise intensity and substrate utilization
restore glycogen stores
absolute fat percentage
interaction between bioenergetics and fuel source
glycogen depletion reduces rate of glycolysis
lowers pyruvate
reliant blood glucose and plasma FFA
lower levels of pyruvate reduced Krebs intermediates and slow Krebs acitvity
decrease in glycogen increase in glycolysis increase n plasma FFA
maintain glycolytic pathways
still need carbohydrates
Contribution of plasma FFA and muscle triglycerides to exercise metabolism during prolonged exercise shows that at beginning of exercise contribution of plasma FFA and muscle triglycerides is equal
As duration of exercise increases there is progressive rise in role of plasma FFA as a fuel source
Carbohydrate storage sites
protein contributes less than 2% of fuel used during exercise of less than 1hr in duration
may increase to 5-10% in longer duration exercise
IMTGs begin to alter ROS
both exercise and nutrition
double whammy
changes genetic expression due to changes in mitochondrial biogenesis
M4 expression of GLUT4 receptors
mitochondrial biogenesis
changes cytochrome oxidase in ETC
carbohydrate restricted training
limitation of these steps of fatigue levels
fasted training - liver glycogen lowered
enhances genes linked to substrate utilization and mitochondrial function
low glycogen (2x/day training)
increase citrate synthase and exercise capacity
1st session burns most of glycogen
don’t restore most stores
citrate synthase is rate limiter of Krebs
can increase glycogen capacity
post exercise CHO restriction
Sleep low - train low
improves gene expression (PGC-1a etc)
greater fat oxidation - similar gene expression
improved cycling efficiently and TT performance
exercise before sleep and then exercise again without fuelling
VO2 in men and women
women have lower absolute VO2max than men
less of a difference when comparing relative VO2max
size and body composition impact VO2
more muscles we use the higher the VO2
when we control for body size the difference between men and women lessens
exercise intensity in makes and females
menstrual cycle is variable
shifts energy consumption and utilization
oral contraceptive use
different types may confound
estrogen blocks and alters epinephrine pathways
important to consider other physiologically relevant factors
body fat percentage
mass
height
pathological differences
lean muscle mass matching to compare
fat does not use as much oxygen
structural components are controlled
fat oxidation in women and men
better in women
increased type 1 fibre %
increased mitochondria, myoglobin and capillary density are designed for aerobic metabolism
preferentially use fatty acids
increases IMCL availability
store more IMCL droplets near mitochondria in type 1 fibres
readily accessible fuel source
increased adipose FFA production
greater lipolysis leasing ot more circulating FFAs
more substrate available for oxidation by muscle
increased FFA oxidative protein expression
high levels of fat transport and oxidation proteins
improves ability to transport FFAs into mitochondria and oxidize them
women have machinery due to increased fat stores
change in estocyles - change in estrogen
lowers RER
impact of exercise intensity on bioenergetics and metabolism
changes in GLUT4 proteins
RER shift
increase or change in TFPalpha
provides or improves lipolysis
cori cycle transporters
lactate transporter
muscle cells ↔ blood ↔ liver
MCTs uptake lactate into the liver
follows concentration gradient
Glucose transort
liver ↔ blood ↔ muscle
pyruvate transport
mitochondrial pyruvate carrier
imports pyruvate into mitochondria for gluconeogensis or TCA cycle activity
McArdle’s syndrome
Genetic disease cannot synthesize phosphorylase enzyme
Prevents breakdown of muscle glycogen as a fuel source during exercise
Prevents muscle from producing lactate
More fat used at submaximal exercise ompared to control
Not able to oxidize more fat
Carbohydrate availability limits fat oxidization even during steady-state exercise
is low intensity exercise best for burning fat
Overal energy expenditure is also very low at low exercise intensities
Only a small amount of fat is oxidized
Fat oxidizartion increases up utni 60% VO2 max before decreasing this means that
The highest rate of fat oxidation seems to appear right before the LT